Influence of confinement on the spreading of bacterial populations
Daniel B. Amchin, Jenna A. Ott, Tapomoy Bhattacharjee, Sujit S. Datta

TL;DR
This paper extends the Keller-Segel model to include confinement effects, revealing how solid obstacles influence bacterial spreading, leading to transitions from chemotactic to growth-driven propagation in crowded environments.
Contribution
It introduces a novel model incorporating confinement effects into bacterial spreading dynamics, aligning with experimental observations and highlighting the transition from chemotactic to growth-driven spreading.
Findings
Confinement hinders chemotactic pulse formation and propagation speed.
Cell-cell collisions become more significant with increased confinement.
Population spreading shifts from chemotactic to growth-driven as confinement intensifies.
Abstract
The spreading of bacterial populations is central to processes in agriculture, the environment, and medicine. However, existing models of spreading typically focus on cells in unconfined settings--despite the fact that many bacteria inhabit complex and crowded environments, such as soils, sediments, and biological tissues/gels, in which solid obstacles confine the cells and thereby strongly regulate population spreading. Here, we develop an extended version of the classic Keller-Segel model of bacterial spreading that incorporates the influence of confinement in promoting both cell-solid and cell-cell collisions. Numerical simulations of this extended model demonstrate how confinement fundamentally alters the dynamics and morphology of spreading bacterial populations, in good agreement with recent experimental results. In particular, with increasing confinement, we find that cell-cell…
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